Aβ42’s signaling to hyperphosphorylate tau also contributes to eventual formation of Aβ deposits and tau-containing neurofibrillary lesions[55,56], because disrupting this signaling via PTI-125 markedly reduces both Aβ deposits and neurofibrillary lesions in 3xTg AD mice or ICV Aβ42-infused wildtype mice[13,15]. This evidence concerns the gene MAPT and Alzheimer disease.